Carnosine release from olfactory bulb synaptosomes is calcium-dependent and depolarization-stimulated.
The dipeptide carnosine (beta-alanyl-L-histidine) has been proposed as a neurotransmitter in the mammalian olfactory pathway. Therefore, the efflux of in vivo-synthesized [14C]carnosine from mouse olfactory bulb synaptosomes was investigated. Carnosine was found to be released from the olfactory bulb synaptosomes by two mechanisms. The first is a slow spontaneous process that is independent of depolarization. The rate of this release was doubled in the presence of 1 mM external carnosine. Release by the second mechanism was markedly stimulated in the presence of calcium by depolarization with either 60 mM K+ or 300 microM veratridine. Omission of calcium abolished the stimulatory effect of both of these agents. Further, blockage of the veratridine-induced depolarization by tetrodotoxin also inhibited carnosine release. These results are consistent with the hypothesis that carnosine acts as a neurotransmitter in the mouse olfactory pathway.
D000818:Animals; D002118:Calcium / Q000494:pharmacology*; D002336:Carnosine / Q000378:metabolism*; D004151:Dipeptides / Q000378:metabolism*; D004298:Dopamine / Q000378:metabolism; D004533:Egtazic Acid / Q000494:pharmacology; D005260:Female; D007425:Intracellular Membranes / Q000502:physiology; D007700:Kinetics; D007930:Leucine / Q000378:metabolism; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D009830:Olfactory Bulb / Q000378:metabolism*; D011188:Potassium / Q000494:pharmacology; D013574:Synaptosomes / Q000187:drug effects / Q000378:metabolism*; D013779:Tetrodotoxin / Q000494:pharmacology; D014701:Veratridine / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D004151:Dipeptides; D013779:Tetrodotoxin; D004533:Egtazic Acid; D005680:gamma-Aminobutyric Acid; D014701:Veratridine; D002336:Carnosine; D007930:Leucine; D011188:Potassium; D002118:Calcium; D004298:Dopamine